Lipid Sensor GPR120 Linked to Obesity in Mice and Humans

Variant of GPR120 which inhibits GPR120 signaling linked with increased risk of obesity

MONDAY, Feb. 20 (HealthDay News) -- A protein that acts as a lipid sensor, GPR120, can lead to obesity when defective in mice and humans, according to a study published online Feb. 19 in Nature.

To examine the role of GPR120, a receptor for unsaturated long-chain free fatty acids known to be critical in physiological processes, including adipogenesis, regulation of appetite, and food preference, Atsuhiko Ichimura, from Kyoto University in Japan, and colleagues studied mice deficient in GPR120 as well as GPR120 expression in humans.

The researchers found that, when the GPR120-deficient mice were fed a high-fat diet, they developed obesity, glucose intolerance, and fatty liver. In addition, they had reduced adipocyte differentiation and lipogenesis but increased hepatic lipogenesis. In humans, GPR120 expression was significantly higher in adipose tissue from obese individuals than lean individuals. Obese individuals carried a deleterious non-synonymous mutation (p.R270H) which inhibited GPR120 signaling. In European populations, this variant was associated with an increased risk of obesity.

"Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents," Ichimura and colleagues conclude.